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Department of Gerontology, Huntington University, Sudbury, ON P3E 2C6, Canada


Medical Sciences Division, Northern Ontario School of Medicine, Sudbury, ON P3E 2C6, Canada


Department of Biology, Department of Chemistry and Biochemistry, Biomolecular Sciences Program, Laurentian University, 935 Ramsey Lake Road, Sudbury, ON P3E 2C6, Canada


Author to whom correspondence should be addressed.

Abstract Oxidative damage is considered to be the primary cause of several aging associated disease pathologies. Cumulative oxidative damage tends to be pervasive among cellular macromolecules, impacting proteins, lipids, RNA and DNA of cells. At a systemic level, events subsequent to oxidative damage induce an inflammatory response to sites of oxidative damage, often contributing to additional oxidative stress. At a cellular level, oxidative damage to mitochondria results in acidification of the cytoplasm and release of cytochrome c, causing apoptosis. This review summarizes findings in the literature on oxidative stress and consequent damage on cells and tissues of the cardiovascular system and the central nervous system, with a focus on aging-related diseases that have well-documented evidence of oxidative damage in initiation and-or progression of the disease. The current understanding of the cellular mechanisms with a focus on macromolecular damage, impacted cellular pathways and gross morphological changes associated with oxidative damage is also reviewed. Additionally, the impact of calorific restriction with its profound impact on cardiovascular and neuronal aging is addressed. View Full-Text

Keywords: oxidative stress; RONS; cardiovascular; aging; brain oxidative stress; RONS; cardiovascular; aging; brain

Autor: Krishnan Venkataraman 1, Sandhya Khurana 2 and T. C. Tai 2,3,*

Fuente: http://mdpi.com/


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